A reaction-triggered luminescent Ce4+/Tb3+ MOF probe for the detection of SO2 and its derivatives.

A reaction-responsive Ce4+/Tb3+ MOF luminescent probe/test strip was designed and synthesized for sensing gaseous sulfur dioxide and sulfite in human serum. A novel sensing principle based on the chemical reaction of Ce4+ with analytes to powerfully sensitize the luminescence of Tb3+ ion has been proposed.

Sulfur dioxide attenuates sepsis-induced cardiac dysfunction via inhibition of NLRP3 inflammasome activation in rats.

OBJECTIVE: Sulfur dioxide (SO2) plays an important role in maintaining homeostasis of cardiovascular system. This study was aimed to investigate cardioprotective effects of SO2 on in the rat and the underlying mechanism. METHODS AND RESULTS: Sepsis model induced by cecal ligation and puncture (CLP) in rats were used. SO2 donor (NaHSO3/Na2SO3, 1:3 M/M) was administered intraperitoneally at a dose of 85 mg/kg. Primary neonatal rat cardiac ventricular myocytes (NRCMs) were stimulated with LPS (1 mg/mL) in presence or absence of different concentrations of SO2 (10, 50 and 100 µmol/L). SO2 donor could restore the decreased levels of SO2 in plasma and heart of septic rats. SO2 exhibited dramatic improvement in cardiac functions. At 24 h after CLP, SO2 treatments decreased the number of TUNEL-positive cells, Bax/Bcl-2 ratio and activity of caspase-3. Moreover CLP-induced inflammatory response was also relieved by SO2. In NRCMs, SO2 could suppress the LPS-induced myocardial injury, leading to an increase in cell viability, a decrease in LDH and apoptotic rate. Western blot showed that the expression of TLR4, NLRP3, and Caspase-1 were obviously increased in myocardial tissue of CLP group or in NRCMs of LPS group, while SO2 significantly inhibited the CLP-induced or LPS-induced TLR4, NLRP3, and Caspase-1 expression. CONCLUSION: SO2 attenuated sepsis-induced cardiac dysfunction likely in association with the inhibiting inflammation via TLR4/NLRP3 signaling pathway.

Determination of reference intervals for umbilical cord arterial and venous blood gas analysis of healthy Thoroughbred foals.

Although umbilical cord blood gas analysis is considered the best way to assess in utero oxygenation in human neonates, there is limited evaluation of this method in equine neonatology. Our objectives were to assess the practicality of obtaining umbilical cord blood gas samples in the field and to determine umbilical cord arterial and venous blood gas reference intervals (RI) for healthy, newborn foals. Thoroughbred foals >320 days gestation from healthy mares with uneventful pregnancies at one stud farm were evaluated. All parturitions were observed, with paired umbilical arterial and venous whole-blood samples obtained immediately following parturition for blood gas and lactate concentrations measured in duplicate. Apgar scores were assigned immediately and 10 min after birth, with all foals subsequently examined on days 1-28 to monitor for development of perinatal asphyxia syndrome. Foals were excluded from analysis based on abnormalities of stage 2 labour, Apgar scores and gross and histological placental assessment. Data was analysed using a Student's t-test, Pearson's correlation and the Robust method with P ≤ 0.05 significant. Umbilical cord samples were simple to obtain with minimal disruption to the foaling environment. Of the n = 34 foals assessed, n = 7 were excluded based on premature placental separation deliveries. The mean time for stage 2 labour and blood gas analysis after parturition was 17.3 ±â€¯5.1 min and 5.0 ±â€¯2.3 min, respectively. RI were identified for umbilical arterial and venous pH (7.19-7.42 vs. 7.34-7.44), PO2 (15.5-48.39 mmHg vs. 16.6-52.7 mmHg), PCO2 (49.5-82.29 mmHg vs. 45.4-63.1 mmHg), SO2 (9.19-76.89% vs. 39.9-84.88%), bicarbonate (27.3-38.7 mmol/l vs. 27.7-37.8 mmol/l), base excess (0.36-12.9 mmol/l vs. 1.97-13.1 mmol/l), TCO2 (28.99-40.3 mmHg vs. 29.0-39.5 mmHg) and lactate (1.4-7.3 mmol/l vs. 1.3-4.9 mmol/l). Umbilical arterial samples had lower pH (P < 0.0001), PO2 (P = 0.002) and SO2 (P < 0.0001) and higher PCO2 (P < 0.0001) and lactate (P < 0.0001) than venous samples. The initial Apgar score was positively correlated to umbilical arterial SO2 (r = 0.4, P = 0.05) and negatively with umbilical arterial TCO2 (r = -0.6, P = 0.004). Overall, umbilical cord sampling was simple and minimally disruptive, with RI obtained for blood gas measurements. RI for umbilical blood gas measurements from a larger population of healthy and unhealthy foals is required to evaluate the accuracy of this method for assessing in utero oxygenation.

Increased Endogenous Sulfur Dioxide Involved in the Pathogenesis of Postural Tachycardia Syndrome in Children: A Case-Control Study.

BACKGROUND: The pathogenesis of postural tachycardia syndrome (POTS) remains unclear. This study aimed to explore the changes and significance of sulfur dioxide (SO2) in patients with POTS. METHODS: The study included 31 children with POTS and 27 healthy children from Peking University First Hospital between December 2013 and October 2015. A detailed medical history, physical examination results, and demographic characteristics were collected. Hemodynamics was recorded and the plasma SO2was determined. RESULTS: The plasma SO2was significantly higher in POTS children compared to healthy children (64.0 ± 20.8 µmol/L vs. 27.2 ± 9.6 µmol/L, respectively, P < 0.05). The symptom scores in POTS were positively correlated with plasma SO2levels (r = 0.398, P < 0.05). In all the study participants, the maximum heart rate (HR) was positively correlated with plasma levels of SO2(r = 0.679, P < 0.01). The change in systolic blood pressure from the supine to upright (ΔSBP) in POTS group was smaller than that in the control group (P < 0.05). The ΔSBP was negatively correlated with baseline plasma SO2levels in all participants (r = -0.28, P < 0.05). In the control group, ΔSBP was positively correlated with the plasma levels of SO2(r = 0.487, P < 0.01). The change in HR from the supine to upright in POTS was obvious compared to that of the control group. The area under curve was 0.967 (95% confidence interval: 0.928-1.000), and the cutoff value of plasma SO2 level >38.17 µmol/L yielded a sensitivity of 90.3% and a specificity of 92.6% for predicting the diagnosis of POTS. CONCLUSIONS: Increased endogenous SO2levels might be involved in the pathogenesis of POTS.

Endogenous sulfur dioxide regulates hippocampal neuron apoptosis in developing epileptic rats and is associated with the PERK signaling pathway.

Epilepsy is among the most common neurological diseases in children. Recurrent seizures can result in hippocampal damage and seriously impair learning and memory functions in children. However, the mechanisms underlying epilepsy-related brain injury are unclear. Neuronal apoptosis is among the most common neuropathological manifestations of brain injury. Endogenous sulfur dioxide (SO2) has been shown to be involved in seizures and related neuron apoptosis. However, the role of endogenous SO2 in epilepsy remains unclear. This study assessed whether endogenous SO2 is involved in epilepsy and its underlying mechanisms. Using a rat epilepsy model induced by an intraperitoneal injection of kainic acid (KA), we found that hippocampal neuron apoptosis was induced in epileptic rats, and the SO2 content and aspartate aminotransferase (AAT) activity in the plasma were increased compared to those in the control group. However, the inhibition of SO2 production by l-aspartate-ß-hydroxamate (HDX) can subvert this response 72h after an epileptic seizure. No difference in apoptosis was observed 7 d after the epileptic seizure in the KA and KA+HDX groups. The protein expression levels of AAT2, glucose-regulated protein 78 (GRP78), pancreatic eIF2 kinase-like ER kinase (PERK) and phospho-PERK (p-PERK) were remarkably elevated in the hippocampi of the epileptic rats, while the HDX treatment was capable of reversing this process 7 d after the epileptic seizure. These results indicate that the inhibition of endogenous SO2 production can alleviate neuronal apoptosis and is associated with the PERK signaling pathway during the initial stages after epileptic seizure, but inhibiting SO2 production only delayed the occurrence of apoptosis and did not prevent neuronal apoptosis in the epileptic rats.

A Water-Soluble Fluorescent Probe for SO2 Derivatives in Aqueous Solution and Serum Based on Phenanthroimidazole Dye.

A water-soluble fluorescent SO2 derivatives probe PI-SO 2 based on a phenanthroimidazole dye, and a sensitive SO2 recognition site, aldehyde was constructed. The probe PI-SO 2 exhibits desirable properties such as high sensitivity, high selectivity and good water-solubility. Significantly, we have demonstrated that the probe PI-SO 2 is suitable for rapidly fluorescence detecting of SO2 derivatives in aqueous solution and serum. The application of the novel probe PI-SO 2 proved that it was not only a useful tool for the detection of SO2 derivatives in vitro, but also a potential assay for investigating the effects of SO2 derivatives, and demonstrating its value in practical applicationin of complex biological samples.

[Health risks for residents of cities with developed copper industry].

The study results stressed considerable contribution of technogenic environmental pollution in cities with developed copper industry into individual health risk of Sverdlovsk region population.

Changes of sulfur dioxide, nuclear factor-κB, and interleukin-8 levels in pediatric acute lymphoblastic leukemia with bacterial inflammation.

BACKGROUND: Bacterial inflammation is a common complication in patients with leukemia, and sulfur dioxide (SO2) is a bioactive molecule in modulating Gram-negative bacilli infection. This study aimed to examine the changes in SO2, nuclear factor-κB (NF-κB), and interleukin-8 (IL-8) levels in pediatric acute lymphoblastic leukemia (ALL) with Gram-negative bacterial inflammation. METHODS: Fifty-five ALL children were enrolled in this study, including 30 males and 25 females, aged 3-13 years, and the median age was 7.8 years. All these children who accepted chemotherapy for ALL were divided into the control group (before chemotherapy), the infection group (after chemotherapy with infection), and the recovery group (the infection was controlled after 1 week). The serum level of SO2 was detected using high performance liquid chromatography with fluorescence assay, and NF-κB and IL-8 levels were measured by enzyme-linked immunosorbent assay (ELISA). Human THP-1 cells were cultured, induced, and differentiated into macrophages, which were divided into five groups and each group was cultured with different stimulators: lipopolysaccharide (LPS) group, LPS+L-aspartate-ß-hydroxamate (HDX) group, LPS+SO2 group, SO2, and control groups. NF-κB level and IL-8 protein contents by ELISA were examined in each group. RESULTS: In comparison with those of the control group, levels of serum SO2, NF-κB, and IL-8 of the infection group were significantly increased (P < 0.05), while those of the recovery group were significantly decreased (P < 0.05). A positive correlation was found between levels of serum SO2 and intracellular NF-κB/IL-8, and the correlation coefficients were 0.671 and 0.798 (P < 0.05), respectively. According to the results found in human THP-1 cells, levels of NF-κB and IL-8 in LPS group were significantly increased compared with those of the control group (P < 0.05); when compared with those in LPS group, levels of NF-κB in LPS+HDX group further increased significantly (P < 0.05); however, the NF-κB levels of LPS+SO2 group decreased significantly (P < 0.05). CONCLUSION: SO2 may play an anti-inflammatory role during the process of inflammation by inhibiting the activation and transcription of NF-κB.

[Correlation between endogenous sulfur dioxide and homocysteine in children with pulmonary arterial hypertension associated with congenital heart disease].

OBJECTIVE: To determine the relationship between the serum sulfur dioxide, homocysteine and the pulmonary arterial pressure in children with congenital heart defects who generated a pulmonary arterial hypertension syndrome (PAH-CHD), and analyze their role in the pathological process of the disease. METHOD: This was a prospective cohort study, children with systemic pulmonary shunt CHD were selected. The patients were divided into three groups: the CHD with no PAH group:n = 20, 10 males, 10 females, 5 with ventricular septal defect (VSD), 8 with atrial septal defect (ASD) and 7 with patent ductus arteriosus (PDA), mean age (1.9 ± 1.8) years; the CHD with mild PAH group:n = 20, 10 males, 10 females, 12 with VSD, 6 with ASD, and 2 with PDA, mean age (1.0 ± 0.8) year; the CHD with moderate or severe PAH group:n = 20, 8 males, 12 females, 12 with VSD, 6 with ASD, and 1 with PDA, 1 with ASD+VSD, mean age (1.8 ± 1.6) year. Twenty healthy children were enrolled from outpatient department as the control group [included 8 males, 12 females, mean age (1.9 ± 1.5) years]. The homocysteine and SO2 concentrations in the serum samples were detected by a modified high performance liquid chromatographic method with fluorescence detection (HPLC-FD), then, multiple comparisons among the groups were performed with analysis of variance, and the pearson correlation. RESULT: The serum homocysteine concentrations were respectively (11.0 ± 2.7) , (11.7 ± 2.5), (12.0 ± 2.1), (14.3 ± 3.2) µmol/L in the control group, CHD with no PAH group, CHD with mild PAH group, and CHD with moderate or severe PAH group. According to the multiple comparisons, the CHD with moderate or severe PAH group had the highest level (P all < 0.05) .While the comparison within the control group, CHD with none PAH group, and CHD with mild PAH group, the differences were not significant (P all > 0.05). The serum sulfur dioxide strength (concentrated as SO3(2-)) were respectively (10.6 ± 2.4), (8.9 ± 2.3), (7.3 ± 2.9), (4.3 ± 2.1) µmol/L in the control group, CHD with none PAH group, CHD with mild PAH group, and CHD with moderate or severe PAH group. CHD with moderate or severe PAH group had the highest level of serum sulfur dioxide (P < 0.05) . The pearson correlation analysis indicated that in the CHD children, the serum homocysteine were positively correlated with the pulmonary arterial pressure (r = 0.481, P < 0.01), while, the sulfur dioxide were negatively correlated with pulmonary arterial pressure (r = -0.553, P < 0.01).In all children, the serum homocysteine levels were negatively correlated with the sulfur dioxide (r = -0.231, P = 0.039). CONCLUSION: The PAH-CHD children had higher homocysteine levels and lower sulfur dioxide levelsl, which demonstrated the disturbance of homocysteine-sulfur dioxide pathway in the sulfur containing amino acids metabolish in the disease. The homocysteine may become a biological marker which reflecting the severities of the PAH-CHD, while the sulfur dioxide can be a new target for the therapy of PAH-CHD.

Dose-dependent effect of sulfur dioxide on brain damage induced by recurrent febrile seizures in rats.

Sulfur dioxide (SO2) regulates many physiological processes. Little is known about its roles in neurological disorders. In this study, we investigated the role of endogenous SO2 in the development of febrile seizures (FS) and related brain damages. In the rat model of recurrent FS, we found that endogenous SO2 in the plasma and hippocampus was increased, accompanied by upregulation of aspartate amino-transferase 1 (AAT1) and AAT2, and neuronal apoptosis and mossy fiber sprouting (MFS) in the hippocampus. Preconditioning with low concentration of SO2 (1-10 µmol/kg) alleviated the neuronal damage, and attenuated neuronal apoptosis and MFS, whereas preconditioning with high concentration of SO2 (100 µmol/kg) or inhibition of AAT aggravated the neuronal damage, and promoted neuronal apoptosis and MFS in hippocampus of rats with recurrent FS. These data indicate that endogenous SO2 is involved in the development of FS and related brain damage. Preconditioning with low concentration of SO2 may protect neurons from toxicity caused by FS.

Effect of plasma treatment on multi-walled carbon nanotubes for the detection of H2S and SO2.

H(2)S and SO(2) are important characteristic gases of partial discharge (PD) generated by latent insulated defects in gas insulated switchgear (GIS). The detection of H(2)S and SO(2) is of great significance in the diagnosis and assessment of the operating status of GIS. In this paper, we perform experiments on the gas sensitivity of unmodified multi-walled carbon nanotubes (MWNTs) and those modified by atmospheric pressure dielectric barrier discharge (DBD) air plasma at different times (30, 60 and 120 s) for H(2)S and SO(2), respectively. The results show that the sensitivity and response time of modified MWNTs to H(2)S are both improved, whereas the opposite effects are observed for SO(2). The modified MWNTs have almost zero sensitivity to SO(2). Thus, the MWNTs modified by atmospheric pressure DBD air plasma present good selectivity to H(2)S, and have great potential in H(2)S detection.

Sulfur dioxide: a novel gaseous signal in the regulation of cardiovascular functions.

The atmospheric pollutant sulfur dioxide (SO(2)) is endogenously generated from the normal metabolism of sulfur-containing amino acids through the aspartate aminotransferase pathway. SO(2) is produced in cardiovascular tissues, and the aspartate aminotransferase mRNA is localized in endothelia and in vascular smooth muscle cells near the endothelial layer. Recent studies explored the physiological and pathophysiological effects of endogenous SO(2) on the cardiovascular system, and various potential mechanisms were found. These discoveries suggest a novel role of endogenous SO(2) in the modulation of the cardiovascular system and provide a basis for new treatments for cardiovascular diseases.

Effects of sulfur dioxide on hypoxic pulmonary vascular structural remodeling.

Hypoxic pulmonary hypertension is a pathophysiological process important in the development of various cardiopulmonary diseases. Recently, we found that sulfur dioxide could be produced endogenously by pulmonary vessels, and that it showed vascular regulatory capabilities. In this paper, we examined the role of sulfur dioxide in hypoxic pulmonary vascular structural remodeling (HPVSR). A total of 48 Wistar rats were divided into six groups. Rats in the hypoxic group, hypoxic+sulfur dioxide group, and hypoxic+hydroxamate group were left under hypoxic conditions, whereas the control group, control+sulfur dioxide group, and control+hydroxamate group rats were left in room air. For each group, we measured the pulmonary arterial pressure, sulfur dioxide content in plasma and lung tissue, glutamate oxaloacetate transaminase 1 and 2 mRNAs, micro- and ultra-structural changes in pulmonary arteries, proliferation of pulmonary smooth muscle cells, vascular collagen metabolism, pulmonary endothelial cell inflammatory response, and pulmonary vascular endothelin-1 production in the rats. In hypoxic rats, the content of sulfur dioxide in plasma and lung tissue decreased significantly in comparison with those in the control groups, and significant pulmonary hypertension, pulmonary vascular structural remodeling, and increased vascular inflammatory response were also observed in hypoxic rats. Sulfur dioxide donor significantly downregulated Raf-1, mitogen-activated protein kinase kinase-1 (MEK-1) and p-ERK/ERK, and inhibited pulmonary vascular smooth muscle cell proliferation, collagen remodeling and pulmonary vascular endothelial cell nuclear factor-kappaB (NF-kappaB), and intercellular adhesion molecule 1 (ICAM-1) expressions. It also prevented pulmonary hypertension and pulmonary vascular structural remodeling in association with the upregulated sulfur dioxide/glutamate oxaloacetate transaminase pathway. Hydroxamate, however, advanced pulmonary hypertension, pulmonary vascular structural remodeling, and inflammatory response of the pulmonary artery in association with a downregulated sulfur dioxide/glutamate oxaloacetate transaminase pathway. The results suggested that sulfur dioxide markedly inhibited Raf-1, MEK-1, and the phosphorylation of extracellular signal-regulated kinase (ERK), and then inhibited pulmonary arterial smooth muscle cell (PASMC) proliferation induced by hypoxia. The downregulated sulfur dioxide/glutamate oxaloacetate transaminase pathway may be involved in the mechanisms responsible for pulmonary hypertension and pulmonary vascular structural remodeling.

[Effect of sulfur dioxide on pulmonary vascular structure of hypoxic pulmonary hypertensive rats].

OBJECTIVE: Hypoxic pulmonary hypertension is an important pathophysiologic process of various cardiovascular diseases. Sulfur dioxide (SO2) was considered as a kind of toxic gas previously, but recent studies suggested that SO2 could act as a key bioactive molecule in the pathogenesis of cardiovascular diseases. Therefore, this study was designed to examine the effect of sulfur dioxide on pulmonary vascular structure of hypoxic pulmonary hypertensive rats treated with SO2 donor substances. METHODS: The rats were randomly divided into 3 groups: control group(n = 8), hypoxic group(n = 8) and hypoxic + SO2 group (n = 10, treated with SO2 donor Na2SO3/NaHSO3). The rats of hypoxic group and hypoxic + SO2 group were under a hypoxic condition for 21 days, while the rats of control group were exposed to room air. The mean pulmonary artery pressure was tested by means of right cardiac catheterization and the content of SO2 in plasma was investigated by high performance liquid chromatography (HPLC). The change in relative medial thickness (RMT) of pulmonary arteries was examined under optical microscope. The ultra-structural changes were observed under a transmission electron microscope. The data were analyzed through one-way analysis of variance (ANOVA) by SPSS 13.0 software. RESULTS: Compared with control group [(2.25 +/- 0.50) kPa], the mean pulmonary artery pressure of hypoxic group [(5.12 +/- 0.51) kPa] raised significantly (t = 5.091, P < 0.01) and RMT of hypoxic group (9.66 +/- 1.27) compared with control group (6.83 +/- 1.57) significantly raised (t = 3.392, P < 0.01). Ultrastructural observation showed the proliferation and degeneration of endothelial cells in small pulmonary arteries in rats with pulmonary hypertension. The internal elastic lamina was irregular. The proliferation of medial smooth muscle cells of arteries was shown at the level of respiratory bronchioles. The collagens also increased. Meanwhile, compared with control group [(33.36 +/- 5.62) micromol/L], the content of SO2 in plasma of hypoxic group [(27.01 +/- 4.17) micromol/L] declined (t = 2.067, P < 0.05). Whereas compared with that of hypoxic group [(5.12 +/- 0.51) kPa], the mean pulmonary artery pressure of hypoxic + SO2 group [(3.94 +/- 0.33) kPa] declined (t = 2.712, P < 0.01) and RMT of hypoxic + SO2 group (6.97 +/- 1.83) decreased compared with hypoxic group (9.66 +/- 1.27) (t = 3.009, P < 0.01). Compared with those of hypoxic group, the pulmonary artery ultrastructural changes in hypoxic group ameliorated obviously after using exogenous sulfur dioxide donor. The endothelial cells became flat and the smooth muscle cells of arteries slightly enlarged and arranged regularly. At the same time, compared with hypoxic group [(27.01 +/- 4.17) micromol/L], the content of SO2 in plasma of hypoxic + SO2 group [(29.89 +/- 4.52) micromol/L] raised (t = 1.263, P > 0.05). CONCLUSION: Sulfur dioxide plays an important role in the regulation of small pulmonary artery structural changes in hypoxic pulmonary hypertensive rats. The hypoxic pulmonary hypertensive damages can be ameliorated significantly after using exogenous SO2 donor.

Increased oxygen administration improves cerebral oxygenation in patients undergoing awake carotid surgery.

BACKGROUND: During regional anesthesia for carotid endarterectomy (CEA), 10% to 15% of patients develop signs of cerebral hypoxia after cross-clamping, manifested as changes in speech, cerebration or contralateral motor power. Reversal of such neurological deficits using administration of 100% O2 has been described. We used near-infrared cerebral oximetry to assess whether 100% O2 reliably improves regional cerebral oxygenation (rSO2) during carotid cross-clamping. METHODS: Sixteen patients undergoing awake CEA were studied. Bilateral rSO2 optodes were applied before the initiation of sedation and the conduct of the regional blockade. Patients received 28% oxygen by Venturi facemask. Perioperative blood pressure was maintained at or within 10% above the patient's normal limits during carotid cross-clamping. After cross-clamping, 100% O2 was administered for 5 min by a close-fitting anesthetic facemask. The O2 mask was then removed and the patient breathed room air. The effects on rSO2 readings and arterial blood gases were observed after each intervention. RESULTS: Data were analyzed for 15 patients. Ipsilateral rSO2 values decreased by 7.4% +/- 5% after carotid cross-clamping. Administration of 100% O2 resulted in an increase in ipsilateral rSO2 in all patients of 6.9% +/- 3.3% (range, 1%-12%) (paired t-test, P < 0.001) over the cross-clamped value while receiving 28% O2. Hemodynamic variables and arterial PaCO2 values were unaltered. CONCLUSION: With the carotid cross-clamped, ipsilateral rSO2 was reliably increased by the administration of 100% O(2) compared with 28% O2. The etiology of this increase is unclear, but may relate to the associated increase in O2 content of the blood or to an improvement in cerebral blood flow. Thus administration of 100% O2 during carotid cross-clamping may be beneficial for all patients undergoing CEA.

Effects of endogenous sulfur dioxide on monocrotaline-induced pulmonary hypertension in rats.

AIM: The present study aimed to explore the protective effect of endogenous sulfur dioxide (SO2) in the development of monocrotaline (MCT)-induced pulmonary hypertension (PH) in rats. METHODS: Forty Wistar rats were randomly divided into the MCT group receiving MCT treatment, the MCT+L-aspartate-beta- hydroxamate (HDX) group receiving MCT plus HDX treatment, the MCT+SO2 group receiving MCT plus SO2 donor treatment, and the control group. Mean pulmonary artery pressure (mPAP) and structural changes in pulmonary arteries were evaluated. SO2 content, aspartate aminotransferase activity, and gene expression were measured. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), reduced glutathione (GSH), oxidized glutathione, and malondialdehyde (MDA) levels were assayed. RESULTS: In the MCT-treated rats, mPAP and right ventricle/(left ventricle+septum) increased significantly (P<0.01), pulmonary vascular structural remodeling developed, and SOD, GSHPx, CAT, GSH, and MDA levels of lung homogenates significantly increased (P<0.01) in association with the elevated SO2 content, aspartate aminotransferase activity, and gene expression, compared with the control rats. In the MCT+HDXtreated rats, lung tissues and plasma SO2 content and aspartate aminotransferase activities decreased significantly, whereas the mPAP and pulmonary vascular structural remodeling were markedly aggravated with the decreased SOD, CAT, and GSH levels of lung tissue homogenates compared with the MCT-treated rats (P<0.01). In contrast, with the use of a SO2 donor, the pulmonary vascular structural remodeling was obviously lessened with elevated lung tissue SOD, GSH-Px, and MDA content, and plasma SOD, GSH-Px, and CAT levels. CONCLUSION: Endogenous SO2 might play a protective role in the pathogenesis of MCT-induced PH and promote endogenous antioxidative capacities.

Operative stress response and energy metabolism after laparoscopic cholecystectomy compared to open surgery.

AIM: To determine the least invasive surgical procedure by comparing the levels of operative stress hormones, response-reactive protein (CRP) and rest energy expenditure (REE) after laparoscopic (LC) and open cholecystectomy (OC). METHODS: Twenty-six consecutive patients with noncomplicated gallstones were randomized for LC (14) and OC (12). Plasma concentrations of somatotropin, insulin, cortisol and CRP were measured. The levels of REE were determined. RESULTS: In the third postoperative day, the insulin levels were lower compared to that before operation (P<0.05). In the first postoperative day, the levels of somatotropin and cortisol were higher in OC than those in LC. After operation the parameters of somatotropin, CRP and cortisol increased, compared to those in the preoperative period in the all patients (P<0.05). In the all-postoperative days, the CRP level was higher in OC than that in LC (7.46+/-0.02; 7.38+/-0.01, P<0.05). After operation the REE level all increased in OC and LC (P<0.05). In the all-postoperative days, the REE level was higher in OC than that in LC (1438.5+/-418.5; 1222.3+/-180.8, P<0.05). CONCLUSION: LC results in less prominent stress response and smaller metabolic interference compared to open surgery. These advantages are beneficial to the restoration of stress hormones, the nitrogen balance, and the energy metabolism. However, LC can also induce acidemia and pulmonary hypoperfusion because of the penumoperitonium it uses during surgery.

Intravenous allicin improves pulmonary blood flow after ischemia-reperfusion injury in rats.

BACKGROUND: Allicin is a sulfur-containing compound extracted from garlic, with antiaggregatory, anti- migratory, anti-oxidant and pulmonary vasodilator actions. We hypothesized that allicin might be beneficial in lung ischemia-reperfusion. METHODS: A non-nothermic rat lung ischemia-reperfusion model was established by clamping left pulmonary artery (PA) for 1 hr, followed by reperfusion for 2 hrs by clamping right PA to reflect solely the function of left lung. Groups were control (n=7), allicin 0.1 mg (n=8) and allicin 0.01 mg (n=4). In the beginning of reperfusion allicin/saline were injected. Pulmonary artery pressures (PAP), pulmonary artery flow (PAF), left atrial pressure (LAP) were monitored. At the end of reperfusion period arterial blood gas (ABG) analysis was done. RESULTS: Six of 7 control and 3 of 8 group 2 animals died before completing the experiment. In group 1 all animals completed the experiment (p=0.015 vs control). PAF was significantly increased after 30, 60 and 120 min of reperfusion in group 1 (p=0.0028, 0.0009, 0.0003 respectively vs control) and after 60 and 120 minutes in group 2 (p=0.0453, 0.018 respectively vs control). Pulmonary vascular resistance was lower at 30 min in allicin 0.01 mg group (p=0.0017 vs control). PAP was increased after 60 and 120 min of reperfusion in group 1 (p=0.016, 0.0029 respectively vs control) and after 120 min in group 2 (p=0.0104 vs control). CONCLUSIONS: This study shows that allicin improves postischemic PAF in this model. Allicin needs further investigation of potential utility and mechanism(s) of action.

[Impact of Brownian motion and magnetic fields of erythrocytes on spin echo signal of blood protons]. / Vliianie brounovskogo dvizheniia i magnitnykh polei éritrotsitov na signal spinovogo ékha protonov krovi.

A reduction in blood So2 and ESR is shown to lead to the decay of a spin echo signal. This effect is explained by the impact of red blood cell magnetic field fluctuations caused by the Brownian motion. The authors propose to use the effect to monitor red blood cell agglutination.